In summary, we uncovered a broader cellular and therapeutic operation mode of FTY720, suggesting beneficial FTY720 effects also on CNS neurons during MS therapy and for treatment of other neurodegenerative diseases requiring neuroprotective and neurorestorative processes.

Figure 1: (A) Outline of the facial nerve lesion model with the facial nerve represented as a solid blue line (at the start), dashed line (degenerating after its cut/axotomy) and red line (after injection of the Flurogold [FG] tracer 15 days following cutting). The facial nucleus (the start of the facial nerve in the brainstem) is stained with anti-FG antibodies to visualize the FG tracer. Fingolimod enhanced the number of FG positive motoneurones on the lesioned side (E) compared to sham/DMSO injected animals (D).

Here, the authors provide more basic science evidence supporting a role for fingolimod in nerve repair, specifically neuronal repair. They demonstrate that fingolimod induces expression of neuronal plasticity associated genes c-Fos, c-FosB, Bdnf, Egr1 and Egr2, as well as genes encoding components of the actin cytoskeleton that make up axons. They also provide in vitro evidence that fingolimod stimulates growth cone filopodia extension in primary neurones (i.e. demonstrating a potential for initiating axonal growth in the CNS) and in vivo evidence that it enhances axonal regeneration of an injured facial nerve (peripheral nerve, see Figure 1). So there may be additional beneficial effects to fingolimod than simply sequestration of auto-reactive immune cells in lymph nodes. But like most findings in science, I don't think contradictory findings in science are senseless in themselves, but a necessary paradox.

“That was excellently observed’, say I, when I read a passage in an
author, where his opinion agrees with mine. When we differ, there I
pronounce him to be mistaken.” - Jonathan Swift (1167-1745).